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Updated: May 17, 2025
Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
Published on: March 11, 2017
Prevotella-Produced Succinate Alleviates Hepatic Steatosis by Enhancing Mitochondrial Function in Layer-Type Chickens
1Key Laboratory of Efficient Utilization of Non-grain Feed Resources (Co-construction by Ministry and Province), Ministry of Agriculture and Rural Affairs, Shandong Provincial Key Laboratory of Animal Nutrition and Efficient Feeding, College of Animal Science and Technology, Shandong Agricultural University, Tai'an, China.
Prevotella bacteria and its metabolite succinate reduce liver fat accumulation in chickens. This occurs by decreasing fatty acid synthase activity and improving mitochondrial function, mediated by the succinate receptor 1 (SUCNR1) pathway.
Area of Science:
- Gut microbiota and host metabolism
- Animal nutrition and physiology
- Hepatic lipid metabolism
Background:
- Prevotella species are linked to high-fiber diets and L-arabinose supplementation.
- The impact of Prevotella and succinate on liver fat is not well understood.
Purpose of the Study:
- To investigate the effects of Prevotella and succinate on hepatic steatosis in layer-type pullets.
- To elucidate the mechanisms by which these factors influence liver lipid metabolism.
Main Methods:
- Layer chickens were fed diets with varying L-arabinose levels or supplemented with Prevotella or sodium succinate.
- Plasma lipids, hepatic lipid accumulation, gene expression, and cecal microbiota were analyzed.
- In vitro studies used chicken embryo hepatocytes treated with Prevotella metabolites or succinate, with or without inhibitors.
Main Results:
- L-arabinose increased Prevotella abundance and reduced hepatic and plasma triglycerides.
- Prevotella and succinate administration decreased plasma triglycerides and hepatic lipid deposition.
- Both Prevotella and succinate suppressed fatty acid synthase activity and enhanced mitochondrial function.
Conclusions:
- Succinate, produced by Prevotella, is a key metabolite reducing hepatic lipid deposition.
- This effect is mediated by suppressing fatty acid synthase and activating mitochondrial function via SUCNR1 and PGC1β.
